骨关节炎中软骨细胞与成骨细胞的协调作用

The Coordinated Role of Chondrocytes and Osteoblasts in Osteoarthritis

摘要: 为明确骨关节炎(OA)进程中软骨细胞与成骨细胞的病理协调机制，本文整合软骨细胞异常活化、成骨细胞表型重塑、软骨–骨细胞串扰、代谢重编程的作用机制，梳理Wnt/β-catenin、NF-κB、TGF-β1、Hedgehog等关键信号通路在软骨基质降解与骨重塑中的作用；分析软骨下骨板孔隙增加、血管侵入等结构改变介导的分子通讯；解析成骨细胞诱导软骨细胞糖酵解增强、软骨细胞Hedgehog信号上调成骨细胞骨保护素(OPG)的实验证据。软骨细胞与成骨细胞通过信号分子、代谢重编程、结构通道形成恶性循环，驱动关节退变，靶向细胞间通讯节点、代谢干预能够为OA提供新型治疗策略。

Abstract: To clarify the pathological coordination mechanism between chondrocytes and osteoblasts during the progression of Osteoarthritis (OA), this paper integrates mechanisms involving abnormal activation of chondrocytes, osteoblast phenotype remodeling, cartilage-bone cell crosstalk, and metabolic reprogramming. Key signaling pathways such as Wnt/β-catenin, NF-κB, TGF-β1, and Hedgehog are reviewed in terms of their roles in cartilage matrix degradation and bone remodeling. The study analyzes molecular communication mediated by structural changes, including increased subchondral bone plate porosity and vascular invasion. Experimental evidence is discussed showing that osteoblasts induce enhanced glycolysis in chondrocytes, while upregulated Hedgehog signaling in chondrocytes stimulates osteoblast production of Osteoprotegerin (OPG). Chondrocytes and osteoblasts form a vicious cycle through signaling molecules, metabolic reprogramming, and structural channels, driving joint degeneration. Targeting intercellular communication nodes and metabolic interventions may provide novel therapeutic strategies for OA.